Schatzker Classification of Tibial Plateau Fractures

The Schatzker classification divides tibial plateau fractures into six types:

Type (%)	Definition	Associated injuries
I (6%)	Lateral plateau fracture without displacement and with less than 4 mm of depression1	May be associated with a distraction-type injury to the medial collateral ligament or anterior cruciate ligament
II (25%)	Lateral plateau fracture with greater than 4 mm of depression	20% of patients have associated distraction injuries to the medial collateral ligament or medial meniscus
IIIA	Compression fracture of the lateral plateau
IIIB	Compression fracture of the central aspect of the tibial plateau	May result in joint instability
IV (10%)	Medial plateau fracture with a split or depressed component	Worst prognosis. Increased likelihood of injury to the peroneal nerve or popliteal vessels. Frequently associated with distraction injury to the lateral compartment2
V (3%)	Bicondylar plateau fracture (wedge fractures of the medial and lateral tibial plateau	Articular depression typically seen in lateral plateau. May see associated fracture of the intercondylar eminence. 50% have peripheral meniscal detachment. 30% have anterior cruciate ligament avulsion injury. Status of soft tissues dictates management.
VI (20%)	Transverse subcondylar fracture with dissociation of the metaphysis from the diaphysis	30% are open. There is frequently extensive soft-tissue injury. Increased risk of compartment syndrome. Status of soft tissues dictates management.

¹ Lateral tibial plateau depression is measured as the vertical distance between the lowest point on the intact medial plateau and the lowest depressed lateral plateau fracture fragment
² e.g., lateral collateral ligament complex injury, posterolateral corner injury, or fracture or dislocation of proximal fibula

References

Markhardt BK, Gross JM, Monu J. Schatzker Classification of Tibial Plateau Fractures: Use of CT and MR Imaging Improves Assessment. RadioGraphics 2009 29:585-597.

Disseminated Pulmonary Ossification

Disseminated pulmonary ossification (DPO) refers to the formation of mature bone in the lung parenchyma. It is usually seen in men between 40 and 60 years of age, predominantly in the lower lobes.

DPO is usually seen in association with chronic heart or lung diseases and has been classified into nodular and branching types. Differential considerations include:

• mitral stenosis and other diseases that cause pulmonary venous hypertension: Most common association. Seen in 15-50% of these patients. The appearance is nodular.
• interstitial pulmonary fibrosis: May be seen in up to 9% of these patients.
• chemotherapy: e.g., busulfan
• hemodialysis
• acromegaly
• metastatic cancer

References

• Luschka H. Verastigte Knockenbildung im Parenchym der Lunge. VirchowsArch [PatholAnat] 1856;10:500-505.
• Gevenois PA, Abehsera M, Knoop C, Jacobovitz D, Estenne M. Disseminated pulmonary ossification in end-stage pulmonary fibrosis: CT demonstration. AJR Am J Roentgenol. 1994 Jun;162(6):1303-4.

Differential Diagnosis of Unilateral Tibial Bowing

Anterolateral bowing

• Neurofibromatosis type 1 (shown above): Can be unilateral. Fibula may or may not be hypoplastic.
• Congenital anterolateral tibial bowing and polydactyly (CATBP)

Anteromedial bowing

• Fibular hemimelia: Linked to the sonic hedge-hog gene. May also see skin dimpling over the tibia, equinovalgus foot, missing lateral toes, and tarsal coalition.

Posteromedial bowing

• Calcaneovalgus foot deformity: resolves with growth. Also associated with limb-length inequality and triceps surae weakness.

Lateral bowing

• Physiologic in infants
• Abnormalities of the medial physis: Fracture malunion, Blount disease, Turner syndrome, rickets, hypophosphatasia
• Fibrocartilaginous dysplasia At the site of pes anserinus tendon insertion.

Special thanks to Dr. James Dimaala for the case of anterolateral tibial bowing in a patient with neurofibromatosis type I.

Rasmussen Encephalitis

Rasmussen encephalitis (RE) is an inflammatory unilateral brain disorder with progressive tissue and function loss and epilepsy.

Patients (mainly, but not exclusively, children) pass through a prodromal period of minor signs and symptoms, followed by the acute stage, characterized by progressive decline of functions associated with the affected hemisphere (hemiparesis, hemianopia, cognitive deterioration and/or aphasia), as well as seizures. About 50% of patients experience epilepsia partialis continua: unilateral myoclonic twitching of the distal extremities or the face for at least 1 hour with intervals of no more than ten seconds. The patient passes into the residual phase of stable neurological deficit and decreased frequency of seizures after about 8 months.

Pathologically, there is infiltration of T lymphocytes. Cytotoxic T-cells are thought to lead to apoptosis of neurons and astrocytes.

Imaging shows progressive unilateral (usually precentral and inferior frontal) atrophy. CT and MRI are often initially normal, followed by findings of cortical swelling and then atrophy. FLAIR may show small areas of hyperintensity that increase over time. MR spectroscopy shows decreased NAA and choline and increased myoinositol and glutamine/glutamate.

Functional imaging (e.g., PET) may reveal decreased activity in the affected lobe(s) or hemisphere when MRI is normal. PET and SPECT may also show crossed cerebellar diaschisis.

Differential considerations include:

• Sturge-Weber syndrome: Also will see progressive hemispheric atrophy, but there may be cortical calcifications and enhancing of pial angiomas. Clinically, there is a port wine facial nevus.
• MELAS: Mitochondrial encephalopathy, lactic acidosis, and strokelike episodes. Will see cortical atrophy in the chronic phase. Look for lacunar infarctions.
• Hemispheric infarction (Dyke-Davidoff-Masson): Will also have unilateral atrophy, but there may be compensatory calvarial thickening, elevation of the petrous ridge and hyperaeration of the paranasal sinuses.

References

Bien CG, Schramm J. Treatment of Rasmussen encephalitis half a century after its initial description: Promising prospects and a dilemma. Epilepsy Res. 2009 Jul 15.

Hemimegalencephaly

Hemimegalencephaly is the hamartomatous overgrowth of all or part of a cerebral hemisphere with defects of cellular organization and neuronal proliferation, migration, and organization. Hemimegalencephaly may be associated with pachygyria, polymicrogyria, heterotopia, and balloon cells.There is usually an inverse relationship between the size of the affected hemisphere and the severity of its malformation.

It has been suggested that hemimegalencephaly is a disorder of the entire brain that is more evident on one side.

Clinical Presentation and Classification

The classical triad is psychomotor retardation, contralateral motor deficit, and epilepsy. Prognosis depends on severity of epilepsy and associated neurological deficits.

Three clinical types have been described:

• Isolated form: The classic and most common type. Sporadic without evidence of cutaneous or systemic involvement
• Systemic form: Associated with partial or total hemigigantism and/or several neurocutaneous syndromes, including epidermal nevus syndrome (sporadic spectrum of disorders that includes linear sebaceous nevus syndrome and the Proteus syndrome)
• Total hemimegalencephaly: The least common form, in which there is involvement of the ipsilateral cerebellum and brainstem.

Imaging

MRI will show the obvious enlargement of one hemisphere, as well as disorders of cortical migration and development, such as agyria, pachygyria, micropolygyria, and lissencephaly. Because the treatment for seizures is hemispherectomy, it is important to also make note of any cortical abnormalities on the contralateral side, as hemispherectomy in such cases would likely not be effective.

MRA may show anomalies of vascular structures, including hypoplasia of the deep venous system, hypertrophy of the veins draining into the sagittal sinus, abnormal extension of the sylvian veins up to longitudinal superior sinus, and arterial hypervascularization of the affected hemisphere

Differential Diagnosis

• Disorders of neuronal migration
• Tuberous sclerosis
• Hemiatrophy
• Gliomatosis cerebri
• Unilateral cortical edema

References

Di Rocco C, Battaglia D, Pietrini D, Piastra M, Massimi L. Hemimegalencephaly: clinical implications and surgical treatment. Childs Nerv Syst. 2006 Aug;22(8):852-66.

Alexander Disease

Alexander disease is a rare, nonfamilial, leukoencephalopathy that is characterized by white matter abnormalities primarily in the frontal lobes.

Three clinical subtypes have been described:

• Neonatal: There is extremely rapid deterioration.
• Infantile: This is the most common. There is early onset macrocephaly and rapid deterioration.
• Adult: The least common and mildest subtype.

On CT, there is low attenuation within the frontal white matter, internal capsule, and caudate heads. There is intense enhancement in early disease in the periventricular rim, frontal lobe white matter, basal ganglia, thalami, brainstem (periaqueductal area), dentate nuclei, fornix, and optic chiasm. MRI shows white matter changes in the frontal white matter. The periventricular rim is high intensity on T1- and low intensity on T2-weighted images.

Colloid Cyst

Colloid cysts are benign, congenital, mucus-containing, epithelium-lined cysts that almost always arise in the anterior third ventricle in the region of the foramina of Monro. They present in the third or fourth decade. The most common symptom is heaache.

CT findings in the characteristic location are usually enough for diagnosis. The attenuation on CT depends on hydration state, but approximately 2/3 demonstrate high attenuation. On T1-weighted images, the signal correlates with cholesterol concentration in the cyst. 2/3 are hyperintense on T1. On T1-weighted images, the signal correlates with water concentration in the cyst. The majority are isointense to brain on T2-weighted images. No suppression or restriction is seen on FLAIR and DWI, respectively. Usually no enhancement is seen.

Atypical Findings

Less than 1% can be seen in the lateral or 4th ventricles, cerebellum, or extraxial space. They are rarely low attenuation. Hemorrhage, enhancement, and calcification are also uncommon findings. About 25% have mixed attenuation/signal. Fluid-fluid levels are also uncommonly seen.